{"id":6555,"date":"2026-06-03T14:05:36","date_gmt":"2026-06-03T18:05:36","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&p=6555"},"modified":"2026-06-09T18:18:37","modified_gmt":"2026-06-09T22:18:37","slug":"adaptive-specific-immunity-t-cells-and-b-cells","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/adaptive-specific-immunity-t-cells-and-b-cells\/","title":{"raw":"Section 8:\u00a0 Adaptive (Specific) Immunity - T Cells and B Cells","rendered":"Section 8:\u00a0 Adaptive (Specific) Immunity – T Cells and B Cells"},"content":{"raw":"

While innate immunity<\/strong> provides immediate, broad protection, adaptive immunity<\/strong> targets specific pathogens and builds long-lasting memory through the production of both Memory T<\/strong> and Memory B cells<\/strong>.\u00a0 Adaptive immunity takes longer to become established than innate immunity as a series of events is required to fully activate the T and B cells responsible for adaptive immunity.\u00a0 The T cells once activated provide cell-mediated immunity<\/strong> in which pathogens are killed directly.\u00a0 B cells provide humoral immunity<\/strong> which involves the production of antibodies<\/strong> that have 3 main roles:\u00a0 (1) neutralizing toxins and pathogens by binding them and preventing contact with healthy cells, (2) opsonization and enhancing the phagocytosis of pathogens, and (3) activating the complement system (and therefore also the inflammatory response).<\/p>\r\n\r\n\r\n[caption id=\"attachment_6696\" align=\"alignnone\" width=\"193\"]\"Antibodies<\/a> Antibodies may inhibit infection by (a) preventing the antigen from binding its target, (b) tagging a pathogen for destruction by macrophages or neutrophils, or (c) activating the complement cascade.[\/caption]\r\n

Antigen-Presenting Cells<\/strong><\/span><\/h3>\r\nAntigen-presenting cells (APC)<\/strong> include macrophages, dendritic cells, and B cells, all of which are able to phagocytose and digest pathogens, producing many pathogen fragments (antigens) that can then be displayed on their cell surfaces in order to stimulate the adaptive immune response by both B and T cells.\r\n\r\n[caption id=\"attachment_6702\" align=\"alignnone\" width=\"300\"]\"An<\/a> An APC, such as a macrophage, engulfs and digests a foreign bacterium. An antigen from the bacterium is presented on the cell surface in conjunction with an MHC II molecule. Lymphocytes of the adaptive immune response interact with antigen-embedded MHC II molecules to mature into functional immune cells.[\/caption]\r\n

CD4+<\/sup> Helper T Cells:\u00a0 Orchestrating the Adaptive Immune Response<\/strong><\/span><\/h3>\r\nOnce the APC has engulfed a pathogen, it matures and migrates to a lymph node to activate CD4+<\/sup> Helper T cells (Th<\/sub> cells)<\/strong> as well as CD8+<\/sup> Cytotoxic cells (Tc<\/sub> cells)<\/strong>.\u00a0 Activated Th<\/sub> cells<\/strong> are responsible for orchestrating the adaptive immune response and play crucial roles in activating both B cells<\/strong> and Tc<\/sub> cells<\/strong>.\r\n\r\nTo activate Th<\/sub> cells, three signals are required:<\/span><\/strong>\r\n\r\n\r\n\r\n\r\n\r\n
Signal 1:<\/span><\/strong>\r\n\r\nNon-Self Antigen Presentation<\/span><\/strong><\/td>\r\nTh<\/sub> cells<\/strong> with a complementary TCR<\/strong> and CD4<\/strong> co-receptors bind to the displayed pathogen antigen - MHC-II complexes on the surface of the APC<\/strong>.\r\n\r\nThe match of TCR<\/strong> to this abnormal antigen<\/strong> and simultaneous confirmation by CD4 binding to the MHC-II portion<\/strong> and stabilization of the bound complex is considered the 1st signal.<\/td>\r\n<\/tr>\r\n
Signal 2:<\/span><\/strong>\r\n\r\nLigand-Receptor Interaction<\/span><\/strong><\/td>\r\nTh<\/sub> cells<\/strong> also have CD28 receptors<\/strong> that need to bind with ligands<\/strong> (CD80 and CD86) on the surface of the APC<\/strong>.\u00a0 This \"second handshake\" is considered the 2nd signal.<\/td>\r\n<\/tr>\r\n
Signal 3:<\/span><\/strong>\r\n\r\nCytokine stimulation<\/span><\/strong><\/td>\r\nThe APC then releases cytokines<\/strong> to stimulate Th<\/sub> cells<\/strong> to become fully active<\/strong> and proliferate,<\/strong> producing active daughter Th<\/sub> cells<\/strong> (through clonal expansion) that circulate and activate Tc<\/sub><\/strong> and B cells<\/strong>.\r\n\r\nNote:\u00a0 While the APC is activating the Th<\/sub> cell, the Th<\/sub> cell signals feedback to the APC known as licensing,<\/strong> which causes the APC to become even more active and upregulate ligands (CD80 and CD86) that it uses to bind and activate Tc<\/sub> cells<\/strong>.<\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table>\r\n*The three signals act as safety checks - if a T cell receives Signal 1, but not Signal 2, it will either become anergic<\/strong> (unresponsive) or undergoes apoptosis<\/strong> to prevent accidental autoimmunity.\r\n\r\nTh<\/sub> cells that are activated and proliferate produce the following daughter cell types:\r\n